The effect of acyclovir on the tubular secretion of creatinine in vitroReportar como inadecuado

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Journal of Translational Medicine

, 8:139

First Online: 30 December 2010Received: 13 August 2010Accepted: 30 December 2010DOI: 10.1186-1479-5876-8-139

Cite this article as: Gunness, P., Aleksa, K. & Koren, G. J Transl Med 2010 8: 139. doi:10.1186-1479-5876-8-139


BackgroundWhile generally well tolerated, severe nephrotoxicity has been observed in some children receiving acyclovir. A pronounced elevation in plasma creatinine in the absence of other clinical manifestations of overt nephrotoxicity has been frequently documented. Several drugs have been shown to increase plasma creatinine by inhibiting its renal tubular secretion rather than by decreasing glomerular filtration rate GFR. Creatinine and acyclovir may be transported by similar tubular transport mechanisms, thus, it is plausible that in some cases, the observed increase in plasma creatinine may be partially due to inhibition of tubular secretion of creatinine, and not solely due to decreased GFR. Our objective was to determine whether acyclovir inhibits the tubular secretion of creatinine.

MethodsPorcine LLC-PK1 and human HK-2 renal proximal tubular cell monolayers cultured on microporous membrane filters were exposed to 2-C creatinine 5 μM in the absence or presence of quinidine 1E+03 μM, cimetidine 1E+03 μM or acyclovir 22 - 89 μM in incubation medium.

ResultsResults illustrated that in evident contrast to quinidine, acyclovir did not inhibit creatinine transport in LLC-PK1 and HK-2 cell monolayers.

ConclusionsThe results suggest that acyclovir does not affect the renal tubular handling of creatinine, and hence, the pronounced, transient increase in plasma creatinine is due to decreased GFR, and not to a spurious increase in plasma creatinine.

Electronic supplementary materialThe online version of this article doi:10.1186-1479-5876-8-139 contains supplementary material, which is available to authorized users.

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Autor: Patrina Gunness - Katarina Aleksa - Gideon Koren


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